Carbon 11–Labeled Pittsburgh Compound B and Carbon 11–Labeled (R)-PK11195 Positron Emission Tomographic Imaging in Alzheimer Disease

Abstract

A definitive diagnosis of Alzheimer disease (AD) relies on the demonstration of β-amyloid (Aβ) plaques and neurofibrillary tangles at autopsy.¹ Microglial activation frequently accompanies Aβ deposition, although the time course of their relationship is unclear.² While the exact time course of Aβ deposition in AD has not been elucidated, evidence gained through a postmortem study of Down syndrome (a condition in which Aβ deposition is always present by age 40 years and dementia is common) and an increasing number of reports using the positron emission tomographic (PET) Aβ imaging agent carbon 11 ([¹¹C])–labeled Pittsburgh Compound B (PiB) suggests that Aβ deposition precedes development of the clinical symptoms of dementia.^3-5 Compared with control subjects, patients with AD show marked retention of [¹¹C]PiB in areas of brain association cortex known to contain large amounts of Aβ deposits in AD.^6-8 Levels of [¹¹C]PiB retention comparable to those seen in some subjects with AD have been observed in the cognitively normal elderly population.^4,5 These and other studies suggest that Aβ deposition precedes significant cognitive decline, although more definitive longitudinal studies in healthy elderly persons are needed to fully characterize the relationship between Aβ deposition and cognitive decline.